Final Viruses Flashcards
(36 cards)
Most DNA viruses are ___sDNA, ____ symmetry, and replicated in the ____
There are 3 enveloped groups that include ___, ___, and ___ and 3 naked groups that include ___, ___, and ____
Exceptions include ____, which is ssDNA instead of dsDNA
Another exception is ____, which is not icoshedral and instead surrounded by a complex structural protein that looks like a box
Also ___ replicates in the cytoplasm rather than the nucleus
All the RNA viruses are ____sRNA, ___ symmetry, replicated in the ___, and ___ (do or do not?) have an envelope
Exceptions include ____ which has dsRNA
____s are naked instead of encapsulated
____s have icosahedral shape instead of helical
___ is shaped like a bullet
____ and ____ have nuclear replication instead of cytoplasm
dsDNA, Icoshedral, nucleus
Envelope = Herpes, Hepadana, and Pox
Naked = PAP -> Papova, Adeno, Parvo
Parvo (One PAR in golf)
Pox (Pox in a BOX)
Pox
SsDNA, helical, cytoplasm, do
Reoviridae
Reoviridae, Picorna, and Calici
Reoviridae, Picorna, Calici, Toga, and Flavi
Rhabdo
Retro and Orthomyxo
Unlike + stranded or - stranded RNA viral replication which uses a ___ dependent ___ polymerase, a retrovirus uses a ___ dependent ___ polymerase to transcribe the RNA back into DNA so it can be incorporated into the host’s genome
RNA dependent RNA polymerase, RNA dependent DNA polymerase
Influenza virus A, B, and C is part of the ____ viruses and causes the ____ characterized by fever, runny nose, cough, myalgias arthralgias (muscle aches), etc
Secondary ___ infections can often occur in high risk group patients like the elderly or immunosuppressed (like staph aureus or strep pneumonia)
If a child is given aspirin while they have the flu (Influenza) then they can develop brain and liver disease called ____ syndrome
Hemagglutinin (HA) and Neuraminidase (NA) are part of the influenza’s virulence factors
___ is needed to cleave the mucin barrier that covers cells to protect them in order to expose sialic acid binding sites beneath
Once exposed, ___ is needed to bind to sialic acid on the RBCs surface and surface of cells in the upper respiratory tract so that they can be adsorped into the host cells
^** In other words, HA and NA work together for infection
Antigenic ___ is when minor changes in HA or NA occur, resulting in ____ of the common flu
Antigenic ___ is when major changes in HA or NA occur, resulting in ____ of influenza and this ONLY occurs in influenzae type ___
H5N1 aka Bird flu which is an avian influenza A virus caused a pandemic threat resulting in a clinical pneumonia with diffuse patchy infiltrates on chest radiograms progressing to consolidation in the lungs and a secondary bacterial infection progressing to RDS
Orthomyxo, ORdinary flu (OR for ORthomyxo)
Bacterial
Reyes
NA
HA
Drift, epidemic
Shift, pandemics, A
Mumps and measles are part of the ____ viruses
Although many similar features to Orthomyxoviridae, these viruses have an ___ protein that causes the infected host cell to fuse together forming multinucleated giant cells (aka syncytial cells)
Although most of these contain HA and NA, which Paramyxoviridae contain no NA or HA glycoproteins and which contains only an HA?
Paramyxo
F protein (fusions)
Respiratory Syncytial virus (RSV), Measles
Parainfluenza, RSV, and Metapneumovirus all cause lower respiratory infections in ____ (aka pneumonia), and upper respiratory infections in ___ (bad colds characterized by rhinitis, pharyngitis, and sinus congestion)
____, which occurs in children and characterized by a stridor and a barking cough due to infection and swelling (narrowing) of the larynx occurs in ____ infections
___ is the NUMBER ONE cause of pneumonia in young children less than 6 months of age and metapneumovirus is the second most common cause on pneumonia in young children but a slightly older age group like 1yr olds
____ gland swelling, testicular inflammation (leading to orchitis), and meningitis and sometimes encephalitis would all be due to ___ virus
Measles aka ___ is first characterized by its prodrome of a VERY high fever, hacking cough, rhinitis, conjunctivitis, photophobia, and malasie
After 3-4 days, if you see small red based blue-white lesions in the mouth called ___, your’e about a day away from developing a rash due to the measles virus and this rash starts at the ___ and goes to the neck and torso and ends at the ____ (**Like dumping paint on someone)
The measels virus disseminates to many organs and the most feared complication is ____ and ____ is a slow form of this caused by the virus that occurs years later
Kids, adults
Coupe, Parainfluenza
RSV
Parotid (parotitis), Mumps
Rubeola
Kopliks, head, feets
Encephalitis, SSPE (Subactue sclerosing panencephalitis)
5 Hep viruses are RNA and the 1 Hep virus that is a DNA virus is Hep ____
ABCDE -> A and E at the ends of the spectrum are transmitted via A (anal) and E (enteric) and BCD and via Blood transmission
ABCDE can ALL have acute viral hepatitis manifestations (which normally include the patient being ____ in color, painful enlarged ___, and high levels of liver enzymes), but ONLY ____ can have chronic viral hepatitis
Hep A is part of the ____ viruses, Hep B is part of the ___ viruses, Hep C is a Flavivirus, and Hep E is a ____ virus
___ has increased AST and ALT and only MILD elevated alkaline phosphatase and GGT
___ has increased alkaline phosphatase and GGT and only MILD elevated AST and ALT
Hep B
Jaundiced, liver, BCD
Picrona, Hepadna, Callci (aka Hepeviridae)
Viral hepatitis
Gallstone (blocking of the bile duct)
Anti-HAV IgM means the Hep A is ___ and Anti-HAV IgG means it is ___
Active, Inactive (aka old)
^** Think G = Gone (no more infection)
The intact HepB virus is called the ____ and it can be broken down to tell us more about the infection
Hep B has ___ antigens if there is a LIVE virus and infection (can be either acute/chronic/carrier),
If there is a LIVE virus, we can use ____ antigens to determine if it is acute (we would see Ig__ anti-HBcAgs) or chronic (we would see Ig___ anti-HBcAgs
If the disease is LIVE, along with being either acute or chronic, it can be VERY infectious or Slightly infectious and ___ antigens if the disease is highly active (high infectivity) and anti-___ antigens the disease has low infectivity
Finally, if a patient has ___, they either have NO active disease, immunity, or cured
Hep B has acute viral hepatitis like all the other Heps, ____ hepatitis which is a sever form of acute hepatitis with destruction of the liver (often seen in patients who have Hep B and then become infected with Hep D as a superinfection, or chronic hepatitis (asymptomatic, persistent, or active forms)
Hep B patients can develop primary hepatocellular ____ or liver ____ (Also Hep ___ Genotype 1 often have these complications since 85% of the time patients with acute viral hepatitis C develop chronic hepatitis C ) due to liver injury from the cell mediated immune system
Dane particle
HBsAg (Hep B Surface Antigens),
HBcAg (Hep B Core Antigen), IgM, IgG
HBeAg, Anti-HBeAg
Anti-HBsAg
Fulminant
Primary hepatocellular carcinomas, cirrhosis, Hep C
Hepatitis ___ can NOT infect unless it has the envelope of hepatitis ___, specifically the HB___Ag
^** If they do infect, a coinfection causes acute hepatitis and if a patient already has chronic Hep B and gets infected with Hep D, it is called a superinfection leading to fulminant hepatitis and cirrhosis
The leading cause of Chronic Hepatitis with 85% of those who have an acute infection developing chronic hepatitis is Hep ___
Hep E is often called Non-HepA since they have the same manifestations and mainly occurs in Asia
D, B, HBsAg
C
Retroviridae include Rous sarcoma virus, HTLV-1, and HIV-1
Rous Sarcoma virus is an ____ transforming virus since it carries intact oncogenes (the src oncogene) within the genome and is integrated into the host DNA via integrase (the sticky ends) to cause malignant transformation
ALL the other retroviridae are Non-acute transforming since they activate host cell proto-oncogenes by integrating viral DNA into a key regulatory area
____ is linked to a paralytic disease that occurs in the tropics (Caribbean islands) called tropical spastic paraparesis
AIDS is caused by the retrovirus HIV (Human immunodeficiency virus) as is characterized by immunosuppression leading to increased opportunistic infections, secondary neoplasms, and neurological manifestations
The main routs of transmission include sexual contact (mainly man to man), parenteral inoculation (intravenous drug abusers, hemophiliacs, or recipients of blood transfusions), and transmission from mother to newborns (during intrapartum from an infected birth canal or peripartum from ingestion of breast milk are the most common)
^** Viral transmission occurs via either
1) Direct inoculation into the blood vessels breached by trauma
2) Infection of dendritic cells or CD4+ cells within the mucosa
Also note that HIV is enhanced via coexisting STDs (especially those associated with genital ulcerations)
^** Include Treponema pallidum, herpes simplex virus, Chlamydia trachomatis, and Neisseria gonorrhoeae
Acute transforming
HTLV-1
HIV is a non-acute transforming human retrovirus that belongs to the lentivirus family
There are two forms (HIV-1 and HIV-2) with HIV-1 being the most common
The HIV structure contains a viral core consisting of the major capsid (virus shell) protein ___, a nucleocapsid protein p7/p9, ___ copies of single stranded viral genomic ___NA, and 3 viral enzymes including ___, ___, and ___
The viral core ^ (What we just talked about above) is surrounded by a matrix protein called ___, which is under the virion envelope that has two glycoproteins called ___ and ___ studded into the viral envelope
The HIV-1 RNA genome has Long terminal repeats (LTRs) involved with sticky ends and promotor/enhancer functions, ___ which codes for the viral core proteins P24/MA/NC, ___ encodes for the 3 enzymes, and ___ genes that code for the glycosylated gp120 and gp41 proteins which are all typical of retroviruses
P24, 2 copies, RNA, protease and reverse transcriptase and integrase
P17, gp120 and gp41
Gag, pol, env (env for envelope)
HIV can infect many tissues but the two major tissues are the immune system and CNS
Profound immune deficiency, primariliy effecting ___-mediated immunity is the hallmark of AIDS and the main mechanism for the HIV infection is from a ___ amount of ____ cells (with moncytes/macrophages and dendritic cells also being targets of the HIV infection since they also contain the CD4 receptor)
As an overview, HIV enters through the mucosal tissues and blood and first infects T cells, along with dendritic cells and macrophages, and then it becomes established in the lymphoid tissues where it can remain latent
The HIV life cycle occurs in multiple steps including
1) Infection of the cells
^** This occurs from the ___ and ___ binding first, followed by a conformational change and then ____ co-receptors ___ or ___ binding to the CD4-gp120 complex
^** Note that CCR5 chemokine co-receptor is a R5 strain of the HIV and is called ___-tropic since it preferentially Infects cells of the monocyte/macrophage lineage
CXCR4 is an X4 strain of HIV and called ___-tropic because it preferentially infects T cells
^** R5 strain dominates in acute infection but overtime X4 accumulates and then becomes dominant
Once the gp120-CD4-Chemokine complex is formed, another conformation change occurs in ___ which exposes a fusion peptide which inserts into the cell membrane of the target cells (monocytes/macrophages or T cells) leading to fusion of the virus with the host cell
Cell-mediated, decreased, CD4+ T helper cells
CD4 and gp120, chemokine CCR5 or CXCR4
M-tropic
T-tropic
Gp41
The HIV life cycle occurs in multiple steps including
1) Infection of the cells (talked about on last notecard)
2) Integration of the provirus into the host cell genome
^** After fusion, the virus core containing the HIV genome enters the cytoplasm of the cell and the HIV RNA genome undergoes ____ leading to synthesis of cDNA aka proviral DNA (double stranded complementary DNA) and in dividing T cells the cDNA circularizes, enters the nucleus, and then integrated into the host genome
HIV is able to infect memory and activated T cells, but has a hard time infecting ___ cells because naive T cells have the enzyme APOBEC3G that causes mutations in the HIV genome once it undergoes reverse transcription… However, once the naive T cells become activated, they lose the enzyme and this is why activated or memory T cells can be infected
3) Activation of viral replication
Now remember, the viral life cycle can only be completed after cell activation, so if a cell was already actively replicating, then it just continues along its path…. However most of the time after the provirus is integrated into the host cell’s genome, it stays there in a latent phase where it is silent for months or years
So in this case above ^ once the cell become activated in most CD4+ T cells, the virus activation results in cell ___
Remember, when a T cell is activated by antigens or cytokines it phosphorylates IKB in the cytoplasm, releasing the inhibition it had on NF-KB and therefore NF-KB is up-regulated and translocates to the nucleus where it sends signals for increased transcription of IL-2 and its receptor occur so that the T cells can proliferate and differentiate…. HOWEVER, when the HIV has infected the nucleus and the infected cell becomes activated by an antigen or cytokine (either from the HIV itself or some other infecting microbe), the NF-KB up regulates and translocates to the nucleus but instead of binding on normal promoter regions in the nucleus, it actually binds to the HIV genome that has NF-KB binding sites (the HIV LTR sticky regions) and this causes the ___ of HIV proviral DNA (HIV DNA provirus -> HIV RNA provirus moves to cytoplasm) and leads to the production of virons and lysis of the cell
^** So in other words, if you have HIV you are at an increased risk for recurrent infections -> recurrent infections cause increased lymphocyte activation and production of pro-inflammatory cytokines -> More cytokines and antigens from microbes stimulates more HIV production from the mechanism we explained above ^ -> More CD4+ T cells undergo lysis and die -> More infection since less T cells -> never ending cycle
4) Production and release of infectious agents
2) Reverse transcription
Naive T cells
3) Lysis
transcription
Like we’ve already talked about, T cell depletion occurs mainly from direct cytopathic effects (lysis) of the replicating virus however some other mechanisms can also cause the loss of T cells including
1) Activation induced cell death where chronic activation of uninfected cells responding to HIV itself or an associated infection that cause the cells to undergo apoptosis
2) Pyroptosis
3) Destruction of lymphoid tissues
4) Loss of immature CD4+ T cells
5) Loss of TH1 responses
Since CD4+ T cells are important for both adaptive and humoral immunity, loss of this effects almost every component of the immune system including lymphopenia (low WBCs), decreased T cell function, altered T cell function, polyclonal B cell activation, and altered monocyte and macrophage functions
We’ve mainly talked about infection of T cells by HIV, but remember macrophages and dendritic cells are also infected
1) Macrophages infected by HIV occurs mainly in the tissues
^** Remember, cell division is needed for nuclear entry and replication for most retroviruses, but HIV can infect and multiply in terminally differentiated non-dividing macrophages due to the viral ___ gene (Aka plays a role in regulating nuclear import of HIV-1 and required for virus replication in non-dividing cells like macrophages)
Also unlike CD4+ T cells, macrophages are resistant to the cytopathic effects of HIV and therefore they can harbor the infection since they don’t lyse like T-cells do and are important for the late stages of HIV infection
2) Dendritic cells (Mucosal and follicular)
^** The ___ dendritic cells become infected by the virus and transport it to the regional lymph nodes where it can then be transferred to CD4+ T cells
____ dendritic cells in the germinal centers of the lymph nodes are potential reservoirs of HIV where they trap the HIV virions due to the dendritic cells FC receptor binding to anti-HIV Abs coated around the virions
1) vpr
2) Mucosal
Follicular
Even though we have been focusing mainly on cell-mediated defects from HIV, B cells also undergo changes….
There is polyclonal ___ (Inhibition or activation?) of B cells leading to B-cell hyperplasia in the germinal centers, hypergammaglobulinemia, bone marrow plasmacytosis, and formation of circulating immune complexes
^** But even though there are a lot of activated B cells, patients with AIDS still cant mount an Ab response to new antigens due to the fact that T-helper cells are decreased and can’t help them become activated, and some other factors…
Along with the immune system, remember we said that the CNS is also affected and here the HIV infects macrophages and microglial cells (M-tropic lineage)
Activation
Once the virus enters through the mucosal epithelia (where it normally comes through), a few subsequent phases occur including
1) ___ syndrome is the clinical presentation of the initial spread of the virus and host response and occurs 3-6 weeks after infection and resolves spontaneously after 2-4 weeks
Symptoms are fever like (soar throat, fever, weight loss, fatigue, possible rash, possible diarrhea, possible vomiting)
^** The primary infection occurs when ___ cells with the CCR-5 chemokine in the mucosal lymphoid tissue becomes infected and large amounts of T cells die
At the same time, dissemination (spreading) of the virus occurs via mucosal dendritic cells taking in the virus and bringing them to the lymph nodes and passing them on the CD4+ T cells via direct contact
^** Here, the HIV undergoes viral replication leading to ___ (viruses in the blood that is measured as ____ levels aka viral load) where it continues its dissemination to the peripheral lymphoid tissues infecting macrophages mainly at first, along with dendritic cells and Helper-T cells
As dissemination occurs, development of host immune responses also happens (anti-viral humoral and cell-mediated along with CD8+ CTLs) and evident by 3-7 weeks after the infection
^** The appearance of CTLs are responsible for the initial containment of the HIV infection
After initial viremia, infected people reach a stead state called the ____ and this can be used as a predictor for the rate of decline of CD4+ T cells and therefore progression of the HIV disease
^** Therefore CD4+ Cell counts and not viral load are the primary clinical measurement used to determine when to start antiretroviral therapy
***So in other words, Viral load tells you the speed that a train is heading towards a cliff and CD4 count tells you where the train is compared to the cliff edge
1) Acute retroviral syndrome
Memory CD4+ T cells
Viremia, HIV-1 RNA levels
Viral set point
Once the virus enters through the mucosal epithelia (where it normally comes through), a few subsequent phases occur including
2) Middle, Chronic phase (most patients are asymptomatic)
^** Here, the virus is now concentrated in lymphoid tissues (mainly the lymph nodes and spleen) where continues HIV replication and CD4-T cell destruction occurs gradually
** Remember, this replication and destruction is occurring in the tissues, not the peripheral blood at the moment, however since CD4 T cells in the tissue are declining, there is less and less going out into the peripheral blood**
Along with a slow decline in the number of CD4+ T cells in both the lymphoid organs (from being destroyed) and the blood (from not enough T cells able to get into circulation), the immune defense system starts to decline as well and therefore the number of HIV infected cells begins to increase
^** The immune system declining is due to the HIV beginning to evade immune detection via destroying CD4+ T cells, antigenic variation, down-regulating class ___ MHCs on infected cells (so that the viral antigens are not recognized by CTLs), and switch from CCR5 to some other chemokine
Since no clinical manifestations of HIV occur during this period, it is called the ____ period and usually lasts about 8 years
Even though most patients are asymptomatic, candidiasis (oral thrush), herpes zoster, mycobacterial tuberculosis, athletes foot, some bacterial infections (H influenzae, S. Pneumoniae, Salmonella, S. Aureus, S. Epidermidis, etc) and some other small opportunistic infections might occur
^***** But these are just constitutional symptoms and do not represent AIDS
Class 1
Clinical latency
Once the virus enters through the mucosal epithelia (where it normally comes through), a few subsequent phases occur including
3) Clinical AIDS
Typically occurs in about 7-10 years and clinical features include long lasting fever (over a month) and weight loss, diarrhea, generalized lymphadenopathy
Also, AIDS indicator diseases including
1) Neurologic diseases and constitutional illness (night sweats, fevers, enlarged lymph nodes, severe weight loss, wasting syndrome)
2) Diseases secondary to the immunodeficiency state such as secondary infection by pathogens and normal flora (opportunistic infections)
Opportunistic infections include
A) The most common opportunistic infection in the US is ___ characterized by cough and hypoxia
B) A common yeast infection with oral thrush and esophagitis is ____
C) Chorioretinitis and blindness, along with esophagitis and diarrhea can be due to the __ virus
D) Mycobacterium tuberculosis and MAC can occur with ___ being the most common cause of Fever of Unknown Origin (FUO) in AIDS patients will a CD4 count less than 50
E) Fever, nausea, vomiting, and meningitis is from ____ and if one sees a mass lesion in the brain with fever, headache, and focal neurological defects it is most likely from ____
F) High risk of developing encapsulated organism infections like ____
G) Severe genital or oral outbreaks can be from ___
H) Chronic diarrhea can be from ____, microsporidia, or Isospora belli
I) Herpes zoseters can develop and EBV can cause ___ characterized by white hair like projections arising from the side of the tongue
A) P. Jiroveci (causes PCP)
B) Candida albicans
C) Cytomegalovirus (CMV)
D) MAC
E) Cryptococcus neoformans, Toxoplasma gondii
F) Streptococcus pneumoniae
G) Herpes simplex virus
H) Cryptosporidium
I) OHL (Oral hairy leukoplakia)
Neoplasms due to AIDS are also common and caused by oncogenic DNA viruses mainly….
****A) ____ is a vascular tumor with red to purple lesions and plaques and nodules that arise all over the body and the most common neoplasm associated with AIDS
^** It is characterized by spindle shaped cells that express markers for both endothelial cells (vascular or lymphatic) and smooth muscle cells; along with chronic inflammatory cell infiltrates
KS is caused by ___ and establishes a latent infection during which spindle cell proliferation and activation, along with prevention of apoptosis occurs… And the activated spindle cells produce proinflammatory and angiogenic factors that recruit inflammatory and neovascular components that lead to the tumor
B) Primary ___-cell ___s (commonly occur in the CNS and therefore present as a brain mass) are caused by tumor cells infected with oncogenic viruses, most commonly ____
^** Unchecked proliferation of B cells infected with oncogenic herpesviruses in the setting of profound T cell depletion can lead to lymphomas such as EBV+ large cell lymphomas or EBV+ Hodgkin lymphomas (associated with a large tissue inflammatory response and Reed-Sternberg cells) or KSHV+ primary effusion lymphoma
^**In a patient with AIDS, they obviously have low T cell counts… Since T cell immunity is required to restrain proliferation of B cells infected with oncogenic viruses like EBV (or KSHV), since it is low, this control is lost
THERE IS A SECOND mechanism that can cause B-cell lymphomas not related to EBV and this can occur in patients who might be receiving HAART and therefore have preserved CD4 T cell counts… This mechanism is due to germinal center B-cell hyperplasia in the setting of early HIV infection due to defective AID enzyme can occur
C) Invasive cancer of the uterine cervix, which can be caused by ___
^** This can also be caused by ___ cancer
A) Kaposi sarcoma (KS)
HHV8 (aka Human Herpes virus 8 aka KSHV aka KS herpesvirus….ALL THE SAME THING)
B) B-cell lymphomas, EBV
C) HPV
Anal (Anal intraepithelial neoplasms)
So if one sees hyperplasia of B cell follicles, it is the ___ stages of HIV infection due to polyclonal B-cell activation and hypergammaglobulinemia seen in HIV patients
As the disease progresses, B-cell proliferation subsides and gives way to severe lymphoid involution (inactivation/shrinkage)… The lymph nodes become atrophic and small and can carry opportunistic infections and eventually the spleen and thymus also become involuted
Early
Multinucleated giant syncytial cells with intranuclear inclusion bodies are seen in members of the ____viridae family (and also seen in the Paramyxoviridae family and retroviridae infections)
The herpes virus migrates up the nerves to the ____ where it resides until it is reactivated
There is a HUGE amount of manifestations that can occur depending on the site of inoculation including
1) ___ (aka ___ sores which are vesicles on the lips and mouth that ulcerate)
2) The number 1 cause of viral ____ in the US causing cell death, brain tissue swelling with fever, headache, and neurological abnormalities
3) Genital herpes
4) Neonatal herpes often occurs when mother has a primary genital herpes infection
5) Herpetic ____ which is an infection of the finger that causes it to become red, hot, painful, and swollen
Herpes
Sensory ganglia
1) Gingivostomatitis, Cold sores
2) Encephalitis
5) Herpetic whitlow
Fever, malaise, and headache followed by a skin rash described as “dew on a rose petal” aka a red base with a fluid filled vesicle on top is seen in ____ that starts on the face and trunk and spreads to the entire body (including the mucous membranes like vagina, pharynx, etc)
This rash can sometimes be confused with small pox however the differences include
1) Chickenpox has ___ lesions that ___ (are or are not?) umbilicated, the lesions are in ____ (different or the same?) stages of development, and lesions on the ___ are more common
2) In contrast, small pox which is a member of the ___ viruses has ___ lesions that ___ (are or are not?) umbilicated, the lesions are in ____ (different or the same?) stages of development, and lesions on the ___ are more common
Once this subsides after about a week, if the patient becomes stressed or has a lowered cell-mediated immunity for some reason, the latent virus that now resides in the dorsal root sensory ganglion (where it will be replicated), moves to the peripheral nerves and this is now the beginning of a ___ virus characterized by a painful skin rash that overlays a SPECIFIC sensory dermatome (dermatome distribution is almost always unilateral)
^** Someone with the shingles can give someone chickenpox since they are the same disease
Varicella (chicken pox)
1) Superficial, are not, different, trunk
2) Pox, Deep hard, are, same, extremities
Zosters (shingles)
Cytomegalovirus has 4 clinical states
1) Asymptomatic, which most patients are (80%)
2) Congenital disease which can cross the BBB and is the most common viral cause of ____, and it can also lead to microcephaly, deafness, seizures, etc
3) CMV Mononucleosis (similar to EBV) characterized by a Monospot ___ Mono which tells us that the mono is due to CMV and NOT EBV
4) Reactivation in immunosuppressed patients
^**In patients that have the reactivation of CMV (Cytomegalovirus) if they have ___ they can get retinitis, colitis, viremia, but NEVER pneumonitis (inflammation of the alveoli)
If they have ____ they can get colitis, viremia, pneumonitis but NEVER retinitis
AKA Marrow transplant = CMV ___nitis and AIDS = CMV ____nitis
2) Mental retardation
3) Monospot negative mono
AIDS
Bone marrow transplant
Pneumonitis, Retinitis
If a patient has fever, chills, sweats, headache, and a very painful pharyngitis; along with an enlarged spleen and lymph nodes, think ____ due to ___
Blood work will reveal high WBC count with ___ lymphocytes and ____ antibodies
The Mono-spot test will be + (if Mono is due to CMV, the mono-spot test will be -)
EBV can also be involved in Burkitt’s lymphoma and nasopharyngeal cancers since it transforms B cells
Infectious mononucleosis, EBV
Atypical, heterophile
